We have found that HTLV-I infected T cells express 10-20 fold more TfR on their surface, but that this is due to a redistribution of the receptor from cytoplasm to surface and not to an increased receptor synthesis. Further, the TfR in these cells is poorly internalized and poorly phosphorylated by phorbol ester. The receptor cannot deliver iron to these cells, which nevertheless require iron for proliferation. Antibodies which prevent iron binding to the TfR still inhibit the growth of these cells.